There is considerable evidence that increased total peripheral resistance associated with human essential and many types of experimental hypertension is due to increased vascular reactivity. However, there is little information concerning the underlying mechanisms that might cause these alterations in reactivity. It has been suggested that a derangement in Ca ions metabolism, resulting in part from an alteration in the level of key phosphoproteins, may cause some of the changes in vascular responsiveness observed in hypertensive rats. In this study, sarcolemmal and sarcoplasmic reticular fractions will be isolated from mesenteric arteries. The rate of Ca ions transport, activities of (Na ion plus K ion ATPase) and Ca ions -ATPase and the associated level of phosphoproteins of these fractions from normotensive and spontaneously hypertensive rats will be studied. These studies will result in a better understanding of the alterations in Ca ions and phosphoprotein regulation that might cause increased vascular reactivity associated with hypertensive and other vascular diseases.